title: Severe burn injury induces a characteristic activation of extracellular signal-regulated kinase 1/2 in spinal dorsal horn neurons.
abstract: We have studied scalding-type burn injury-induced activation of extracellular signal-regulated kinase 1/2 (ERK1/2) in the spinal dorsal horn, which is a recognised marker for spinal nociceptive processing. At 5min after severe scalding injury to mouse hind-paw, a substantial number of phosphorylated ERK1/2 (pERK1/2) immunopositive neurons were found in the ipsilateral dorsal horn. At 1h post-injury, the number of pERK1/2-labelled neurons remained substantially the same. However, at 3h post-injury, a further increase in the number of labelled neurons was found on the ipsilateral side, while a remarkable increase in the number of labelled neurons on the contralateral side resulted in there being no significant difference between the extent of the labelling on both sides. By 6h post-injury, the number of labelled neurons was reduced on both sides without there being significant difference between the two sides. A similar pattern of severe scalding injury-induced activation of ERK1/2 in spinal dorsal horn neurons over the same time-course was found in mice which lacked the transient receptor potential type 1 receptor (TRPV1) except that the extent to which ERK1/2 was activated in the ipsilateral dorsal horn at 5 min post-injury was significantly greater in wild-type animals when compared to TRPV1 null animals. This difference in activation of ERK1/2 in spinal dorsal horn neurons was abolished within 1h after injury, demonstrating that TRPV1 is not essential for the maintenance of ongoing spinal nociceptive processing in inflammatory pain conditions in mouse resulting from at least certain types of severe burn injury.
authors.affiliation: Section of Anaesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Chelsea and Westminster Hospital, 369, Fulham Road, London SW10 9NH, United Kingdom.
authors.forename: John P M
authors.initials: JP
authors.lastname: White
authors.forename: Chin Wing
authors.initials: CW
authors.lastname: Ko
authors.forename: Antonio Rei
authors.initials: AR
authors.lastname: Fidalgo
authors.forename: Mario
authors.initials: M
authors.lastname: Cibelli
authors.forename: Cleoper C
authors.initials: CC
authors.lastname: Paule
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Anderson
authors.forename: Celia
authors.initials: C
authors.lastname: Cruz
authors.forename: Szabolcs
authors.initials: S
authors.lastname: Gomba
authors.forename: Klara
authors.initials: K
authors.lastname: Matesz
authors.forename: Gabor
authors.initials: G
authors.lastname: Veress
authors.forename: Antonio
authors.initials: A
authors.lastname: Avelino
authors.forename: Istvan
authors.initials: I
authors.lastname: Nagy
mesh_terms: D000818:Animals; D002056:Burns / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D005260:Female; D008297:Male; D051379:Mice; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism*; D010146:Pain / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D020671:Posterior Horn Cells / Q000378:metabolism*; D012867:Skin / Q000378:metabolism
chemical_list: D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3